About the book
Nephritis can be seen as hereditary or as a result of infection, immunological diseases, metabolic disorders, exposure to toxic factors, and glomerular or hematological diseases. It may be asymptomatic or accompanied by hypertension, renal tubular acidosis, proteinuria, hematuria, edema, anemia, glucosuria, and nocturia. It is a progressive and chronic disease with sometimes acute exacerbations. Chronic nephritis often leads to chronic kidney disease, causing tubular atrophy and interstitial fibrosis. It is seen in approximately 15% of the causes of end-stage kidney disease. Generally, the pathological findings are tubular atrophy and dilatation, fibrosis in the interstitial space, and inflammatory cell infiltration, mostly consisting of mononuclear cells. In the later stages of the disease, glomerulosclerosis and vascular sclerosis develop. Current treatment involves diagnosing and eliminating the causative factor of chronic interstitial nephritis and treating complications according to the extent of kidney damage, the treatment of chronic nephritis is difficult, and the prognosis is poor; treatment is aimed at the etiology. The search for antifibrotic treatment continues in experimental models; various hormones, immunosuppressants, and symptomatic treatments are given according to the degree of renal damage and complications. However, since these treatments are applied for a long time, they cause many complications in the patient.
Nephrotic syndrome is one of the most common chronic diseases of childhood in which many symptoms due to kidney damage are seen together. Massive proteinuria, hypoalbuminemia, hyperlipidemia, lipiduria, and edema are observed in the patient's clinic. 90% of childhood nephrotic syndrome cases are due to primary idiopathic or minimal change disease. It is often seen in adults due to focal segmental glomerulosclerosis, membranous nephropathy, lupus, or diabetes.
While histopathologically, the most common minimal change disease is focal segmental glomerulosclerosis, membranoproliferative glomerulonephritis, mesangial proliferation, proliferative glomerulonephritis, and membranous glomerulopathy can be seen. Treatment is planned according to symptoms, complications, and primary disease. The first goal is to minimize protein loss. Although corticosteroids are the first choice in treatment, if side effects occur or the disease does not respond, immunosuppressive treatments are applied. Current treatment approaches have shown promising results in terms of disease treatment. However, its long-term side effects and remission sustainability are still unclear.
Nephrosis is an inflammatory, neoplastic or non-vascular nephropathy that causes degenerative changes and solute accumulation in tubules and glomeruli. Nephrosis may be due to a primary cause or secondary to another disorder. Nephrosis is often seen as amyloid nephrosis and osmotic nephrosis. Osmotic nephrosis causes structural changes with intracytoplasmic vacuolization and swelling of tubular cells, occurring primarily in the proximal tubules, without a change in osmotic balance, resulting from certain solutes such as dextran, contrast dyes, mannitol, and hydroxyethyl starch. It can lead to clinical manifestations ranging from acute renal failure to chronic kidney disease.
Amyloid light-chain amyloidosis is the most common type of amyloidosis, with the kidney one of the organs most commonly affected. With the enlargement of the kidney area affected by amyloid deposits, proteinuria and renal dysfunction are usually observed. This topic includes advances in research on the etiology and pathogenesis of nephritis, nephrotic syndrome, and nephrosis, new early diagnosis methods, follow-up and treatment plans, and case series. It will provide significant opportunities and support to scientists, philosophic and medical doctors, urologists, nephrologists, public health practitioners, and family physicians from around the world to share new research, ideas, and solutions.
